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Genome-wide Generation and Systematic Phenotyping of Knockout Mice Reveals New Roles for Many Genes CELL White, J. K., Gerdin, A., Karp, N. A., Ryder, E., Buljan, M., Bussell, J. N., Salisbury, J., Clare, S., Ingham, N. J., Podrini, C., Houghton, R., Estabel, J., Bottomley, J. R., Melvin, D. G., Sunter, D., Adams, N. C., Tannahill, D., Logan, D. W., MacArthur, D. G., Flint, J., Mahajan, V. B., Tsang, S. H., Smyth, I., Watt, F. M., Skarnes, W. C., Dougan, G., Adams, D. J., Ramirez-Solis, R., Bradley, A., Steel, K. P. 2013; 154 (2): 452-464

Abstract

Mutations in whole organisms are powerful ways of interrogating gene function in a realistic context. We describe a program, the Sanger Institute Mouse Genetics Project, that provides a step toward the aim of knocking out all genes and screening each line for a broad range of traits. We found that hitherto unpublished genes were as likely to reveal phenotypes as known genes, suggesting that novel genes represent a rich resource for investigating the molecular basis of disease. We found many unexpected phenotypes detected only because we screened for them, emphasizing the value of screening all mutants for a wide range of traits. Haploinsufficiency and pleiotropy were both surprisingly common. Forty-two percent of genes were essential for viability, and these were less likely to have a paralog and more likely to contribute to a protein complex than other genes. Phenotypic data and more than 900 mutants are openly available for further analysis. PAPERCLIP:

View details for DOI 10.1016/j.cell.2013.06.022

View details for Web of Science ID 000321950700020

View details for PubMedID 23870131

View details for PubMedCentralID PMC3717207